HYPOPROLACTINEMIA DOES NOT PREVENT RESTORATION OF NORMAL SPERMATOGENESIS IN GONADOTROPIN-SUPPRESSED, TESTOSTERONE-REPLACED RATS

We have previously shown that suppression of gonadotropins and spermat ogenesis can be produced in rats by immunization against gonadotropin releasing hormone (GnRH). Administration of testosterone (T) alone is effective in restoring complete spermatogenesis in these rats, althoug h it is not effective in doing so in chronically treated hypophysectom ized rats. This suggests that a pituitary factor(s) other than luteini zing hormone (LH) and follicle-stimulating hormone (FSH) is required t o restore normal spermatogenesis. The studies described herein test th e hypothesis that prolactin (PRL) is the additional requirement for co mplete restoration of spermatogenesis. Twenty rats were immunized agai nst GnRH, and four groups of five each received either 1) 24-cm T-fill ed Silastic implant (TSI), 2) TSI plus bromocriptine pellet (B), 3) B plus empty Silastic implant (SI), or 4) SI alone. Five nonimmunized ra ts received Si alone and served as controls. All rats were sacrificed 2 months after treatment. GnRH immunization and B administration suppr essed gonadotropins and PRL levels, respectively, and advanced spermat ids were not detectable in these rats. Testis weight was suppressed to about 19% of controls. The number of advanced spermatids in control r ats was 220 +/- 23 x 10(6). TSI administration restored advanced sperm atids to numbers comparable to controls in GnRH-immunized rats whether the rat received B (191 +/- 17 x 10(6)) or not (217 +/- 78 x 10(6)). Additionally, we determined mRNA levels for PRL and FSH beta subunit ( FSH beta) in the pituitary by Northern blot and densitometric scanning . The mRNA levels of PRL mirrored serum PRL levels, and the same was t rue for FSH beta subunits and serum FSH levels. These data show that s uppression of PRL has no effect on the ability of T to restore complet e spermatogenesis in GnRH-immunized rats. This observation mitigates a gainst the hypothesis that PRL is the pituitary factor required to all ow complete restoration of spermatogenesis to occur.